分支杆菌Rv0024诱导生物膜的形成和抗细胞壁作用研究进展

Progress on Rv0024 Induced Biofilm Formation and Resistance against Cell Wall Acting in Mycobacterium

多药耐药结核菌和广泛耐药结核菌的出现,使得结核病成为全球第二大传染病。而生物膜的形成在几个人类病原体发病机制作用是公认的。然而,在结核分支杆菌感染情况下生物膜的作用和生物膜形成的遗传因素仍然存在很大程度上的未知。论文通过查阅大量外文文献阐述了细胞壁在结核分支杆菌中的耐药机制,并且发现生物膜中Rv0024为新的NlpC/p60蛋白质家族的一员,通过结核分支杆菌Rv0024异位表达,编码一个假定的肽酶,并且随着抗结核药物异烟肼和吡嗪酰胺耐药性的出现,生物膜形成的Rv0024也显著增加。Rv0024可能在初次感染过程中发挥了关键作用,参与宿主细胞的耐药性产生。因此,Rv0024可作为治疗肺结核的一个潜在的药物靶标进行深入研究。

Along with the emergence of multidrug-resistant tuberculosis and extensively drug-resistant tuberculosis,tuberculosis has become the world＇s second largest infectious disease, Role of biofilms in the pathogenesis of several human pathogens is well established.However,in case of Mycobacterium tuberculosis （MTB） infection, the role of biofilms and the genetic requirements for biofilm formation remains largely unknown.In this paper,we refer to a large number of foreign literature and expound the resistance mechanism of cell wall in Mycobacterium tuberculosis, discovery of Rv0024 as a member of the new NlpC/p60 protein family,the expression of MTB Rv0024, encoding a putative peptidoglycan amidase.Along with the emergence of drug resistance and antituberculosis drug isoniazid and pyrazinamide,the biofilm formation of Rv0024 also increased significantly.Rv0024 may play a critical role in initial infection process,adherence to host cells and drug resistance.Thus,Rv0024 may be considered as a potential drug target for the treatment of tuberculosis.